Additional file 1 of Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice

Additional file 1. Fig. S1 Verification of mouse strains generation and PCR genotyping. Fig. S2 FBXL6 enhances KRAS activity by K63-linked polyubiquitination. Fig. S3 Fbxl6 knockout counteract KrasG12D-driven hepatocarcinogenesis. Fig. S4 Triap1 interacts with Prelid2 and enhances its protein stability. Fig. S5 PRELID2 is a poor prognostic biomarker in HCC patients. Fig. S6 Knockdown of Prelid2 suppresses the growth of HCC xenograft tumors. Table S1 PCR primers used for transgenic mice genotyping. Table S2 PCR primers for site-directed mutagenesis. Table S3 Sequences of siRNAs. Table S4 Primers for qPCR. Table S5 Sequences of shRNAs. Table S6 Relationships between PRELID2 and clinicopathologic characteristics in 129 HCC patients of the IHC cohort [n(%)]. Table S7 Relationships between PRELID2 and clinicopathologic characteristics of HCC patients in the 365 HCC patient of TCGA database [n(%)]. Table S8 Univariate and multivariate analyses indicating associations between overall survival and various risk factors in the 129 HCC patients of IHC cohort. Table S9 The relationship between co-expression of FBXL6/p-ERK and clinicopathological features in 118 HCC patients of IHC cohort [n(%)]. Table S10 Univariate and multivariate analyses indicating associations between overall survival and various risk factors in the 118 HCC patients of IHC cohort.